CD8+ cytotoxic T lymphocytes in cancer immunotherapy: A review
CD8+ cytotoxic T lymphocytes (CTLs) are preferred immune cells for targeting cancer. During cancer progression, CTLs encounter dysfunction and exhaustion due to immunerelated tolerance and immunosuppression within the tumor microenvironment (TME), with all favor adaptive immune‐resistance. Cancer‐as...
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| Published in | Journal of cellular physiology Vol. 234; no. 6; pp. 8509 - 8521 |
|---|---|
| Main Authors | , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Wiley Subscription Services, Inc
01.06.2019
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| Subjects | |
| Online Access | Get full text |
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| Abstract | CD8+ cytotoxic T lymphocytes (CTLs) are preferred immune cells for targeting cancer. During cancer progression, CTLs encounter dysfunction and exhaustion due to immunerelated tolerance and immunosuppression within the tumor microenvironment (TME), with all favor adaptive immune‐resistance. Cancer‐associated fibroblasts (CAFs), macrophage type 2 (M2) cells, and regulatory T cells (Tregs) could make immunologic barriers against CD8
+ T cell‐mediated antitumor immune responses. Thus, CD8
+ T cells are needed to be primed and activated toward effector CTLs in a process called tumor immunity cycle for making durable and efficient antitumor immune responses. The CD8
+ T cell priming is directed essentially as a corroboration work between cells of innate immunity including dendritic cells (DCs) and natural killer (NK) cells with CD4
+ T cells in adoptive immunity. Upon activation, effector CTLs infiltrate to the core or invading site of the tumor (so‐called infiltrated–inflamed [I–I] TME) and take essential roles for killing cancer cells. Exogenous reactivation and/or priming of CD8
+ T cells can be possible using rational immunotherapy strategies. The increase of the ratio for costimulatory to coinhibitory mediators using immune checkpoint blockade (ICB) approach. Programmed death‐1 receptor (PD‐1)–ligand (PD‐L1) and CTL‐associated antigen 4 (CTLA‐4) are checkpoint receptors that can be targeted for relieving exhaustion of CD8
+ T cells and renewing their priming, respectively, and thereby eliminating antigen‐expressing cancer cells. Due to a diverse relation between CTLs with Tregs, the Treg activity could be dampened for increasing the number and rescuing the functional potential of CTLs to induce immunosensitivity of cancer cells.
Tumors have specific mechanisms to break T cell responses. CD8+ T cells are the key immune cells for killing cancer cells presenting major histocompatibility complex (MHC) class I molecules. For pursuing this purpose, the cells must first be primed by their cardinal interactions with dendritic cells (DCs), natural killer (NK) cells, and CD4
+ T cells, among them play essential roles for this priming. Then, the primed cells are activated to form effector cytotoxic T lymphocytes (CTLs) for killing cancer cells via release of granules or induction of FasL‐mediated apoptosis. In the established tumors, however, the function of these key effector cells is suppressed by immunosuppressive cross‐talking between cancer cells with tumor stromal cells like cancer‐associated fibroblasts (CAFs), regulatory T cells (Tregs), and macrophage type 2 (M2) cells. CTL‐based therapy can distract cancer cells, and the density of CD8
+ T cells infiltrated to the invasive site of tumor is a predictive marker for influencing the outcomes of immune checkpoint blockade (ICB) blockade therapy. It is suggested to use a combination of immunotherapeutic approaches for rescuing the exhausted CTLs and switching them toward their active effector profile for retaining immunoactivation within the tumor microenvironment (TME) for combatting tumors and enhancing the efficacy of chemo or radiotherapeutic approaches. |
|---|---|
| AbstractList | CD8+ cytotoxic T lymphocytes (CTLs) are preferred immune cells for targeting cancer. During cancer progression, CTLs encounter dysfunction and exhaustion due to immunerelated tolerance and immunosuppression within the tumor microenvironment (TME), with all favor adaptive immune‐resistance. Cancer‐associated fibroblasts (CAFs), macrophage type 2 (M2) cells, and regulatory T cells (Tregs) could make immunologic barriers against CD8+ T cell‐mediated antitumor immune responses. Thus, CD8+ T cells are needed to be primed and activated toward effector CTLs in a process called tumor immunity cycle for making durable and efficient antitumor immune responses. The CD8+ T cell priming is directed essentially as a corroboration work between cells of innate immunity including dendritic cells (DCs) and natural killer (NK) cells with CD4+ T cells in adoptive immunity. Upon activation, effector CTLs infiltrate to the core or invading site of the tumor (so‐called infiltrated–inflamed [I–I] TME) and take essential roles for killing cancer cells. Exogenous reactivation and/or priming of CD8+ T cells can be possible using rational immunotherapy strategies. The increase of the ratio for costimulatory to coinhibitory mediators using immune checkpoint blockade (ICB) approach. Programmed death‐1 receptor (PD‐1)–ligand (PD‐L1) and CTL‐associated antigen 4 (CTLA‐4) are checkpoint receptors that can be targeted for relieving exhaustion of CD8+ T cells and renewing their priming, respectively, and thereby eliminating antigen‐expressing cancer cells. Due to a diverse relation between CTLs with Tregs, the Treg activity could be dampened for increasing the number and rescuing the functional potential of CTLs to induce immunosensitivity of cancer cells. CD8 cytotoxic T lymphocytes (CTLs) are preferred immune cells for targeting cancer. During cancer progression, CTLs encounter dysfunction and exhaustion due to immunerelated tolerance and immunosuppression within the tumor microenvironment (TME), with all favor adaptive immune-resistance. Cancer-associated fibroblasts (CAFs), macrophage type 2 (M2) cells, and regulatory T cells (Tregs) could make immunologic barriers against CD8 T cell-mediated antitumor immune responses. Thus, CD8 T cells are needed to be primed and activated toward effector CTLs in a process called tumor immunity cycle for making durable and efficient antitumor immune responses. The CD8 T cell priming is directed essentially as a corroboration work between cells of innate immunity including dendritic cells (DCs) and natural killer (NK) cells with CD4 T cells in adoptive immunity. Upon activation, effector CTLs infiltrate to the core or invading site of the tumor (so-called infiltrated-inflamed [I-I] TME) and take essential roles for killing cancer cells. Exogenous reactivation and/or priming of CD8 T cells can be possible using rational immunotherapy strategies. The increase of the ratio for costimulatory to coinhibitory mediators using immune checkpoint blockade (ICB) approach. Programmed death-1 receptor (PD-1)-ligand (PD-L1) and CTL-associated antigen 4 (CTLA-4) are checkpoint receptors that can be targeted for relieving exhaustion of CD8 T cells and renewing their priming, respectively, and thereby eliminating antigen-expressing cancer cells. Due to a diverse relation between CTLs with Tregs, the Treg activity could be dampened for increasing the number and rescuing the functional potential of CTLs to induce immunosensitivity of cancer cells. CD8+ cytotoxic T lymphocytes (CTLs) are preferred immune cells for targeting cancer. During cancer progression, CTLs encounter dysfunction and exhaustion due to immunerelated tolerance and immunosuppression within the tumor microenvironment (TME), with all favor adaptive immune‐resistance. Cancer‐associated fibroblasts (CAFs), macrophage type 2 (M2) cells, and regulatory T cells (Tregs) could make immunologic barriers against CD8 + T cell‐mediated antitumor immune responses. Thus, CD8 + T cells are needed to be primed and activated toward effector CTLs in a process called tumor immunity cycle for making durable and efficient antitumor immune responses. The CD8 + T cell priming is directed essentially as a corroboration work between cells of innate immunity including dendritic cells (DCs) and natural killer (NK) cells with CD4 + T cells in adoptive immunity. Upon activation, effector CTLs infiltrate to the core or invading site of the tumor (so‐called infiltrated–inflamed [I–I] TME) and take essential roles for killing cancer cells. Exogenous reactivation and/or priming of CD8 + T cells can be possible using rational immunotherapy strategies. The increase of the ratio for costimulatory to coinhibitory mediators using immune checkpoint blockade (ICB) approach. Programmed death‐1 receptor (PD‐1)–ligand (PD‐L1) and CTL‐associated antigen 4 (CTLA‐4) are checkpoint receptors that can be targeted for relieving exhaustion of CD8 + T cells and renewing their priming, respectively, and thereby eliminating antigen‐expressing cancer cells. Due to a diverse relation between CTLs with Tregs, the Treg activity could be dampened for increasing the number and rescuing the functional potential of CTLs to induce immunosensitivity of cancer cells. Tumors have specific mechanisms to break T cell responses. CD8+ T cells are the key immune cells for killing cancer cells presenting major histocompatibility complex (MHC) class I molecules. For pursuing this purpose, the cells must first be primed by their cardinal interactions with dendritic cells (DCs), natural killer (NK) cells, and CD4 + T cells, among them play essential roles for this priming. Then, the primed cells are activated to form effector cytotoxic T lymphocytes (CTLs) for killing cancer cells via release of granules or induction of FasL‐mediated apoptosis. In the established tumors, however, the function of these key effector cells is suppressed by immunosuppressive cross‐talking between cancer cells with tumor stromal cells like cancer‐associated fibroblasts (CAFs), regulatory T cells (Tregs), and macrophage type 2 (M2) cells. CTL‐based therapy can distract cancer cells, and the density of CD8 + T cells infiltrated to the invasive site of tumor is a predictive marker for influencing the outcomes of immune checkpoint blockade (ICB) blockade therapy. It is suggested to use a combination of immunotherapeutic approaches for rescuing the exhausted CTLs and switching them toward their active effector profile for retaining immunoactivation within the tumor microenvironment (TME) for combatting tumors and enhancing the efficacy of chemo or radiotherapeutic approaches. CD8 + cytotoxic T lymphocytes (CTLs) are preferred immune cells for targeting cancer. During cancer progression, CTLs encounter dysfunction and exhaustion due to immunerelated tolerance and immunosuppression within the tumor microenvironment (TME), with all favor adaptive immune‐resistance. Cancer‐associated fibroblasts (CAFs), macrophage type 2 (M2) cells, and regulatory T cells (Tregs) could make immunologic barriers against CD8 + T cell‐mediated antitumor immune responses. Thus, CD8 + T cells are needed to be primed and activated toward effector CTLs in a process called tumor immunity cycle for making durable and efficient antitumor immune responses. The CD8 + T cell priming is directed essentially as a corroboration work between cells of innate immunity including dendritic cells (DCs) and natural killer (NK) cells with CD4 + T cells in adoptive immunity. Upon activation, effector CTLs infiltrate to the core or invading site of the tumor (so‐called infiltrated–inflamed [I–I] TME) and take essential roles for killing cancer cells. Exogenous reactivation and/or priming of CD8 + T cells can be possible using rational immunotherapy strategies. The increase of the ratio for costimulatory to coinhibitory mediators using immune checkpoint blockade (ICB) approach. Programmed death‐1 receptor (PD‐1)–ligand (PD‐L1) and CTL‐associated antigen 4 (CTLA‐4) are checkpoint receptors that can be targeted for relieving exhaustion of CD8 + T cells and renewing their priming, respectively, and thereby eliminating antigen‐expressing cancer cells. Due to a diverse relation between CTLs with Tregs, the Treg activity could be dampened for increasing the number and rescuing the functional potential of CTLs to induce immunosensitivity of cancer cells. CD8+ cytotoxic T lymphocytes (CTLs) are preferred immune cells for targeting cancer. During cancer progression, CTLs encounter dysfunction and exhaustion due to immunerelated tolerance and immunosuppression within the tumor microenvironment (TME), with all favor adaptive immune-resistance. Cancer-associated fibroblasts (CAFs), macrophage type 2 (M2) cells, and regulatory T cells (Tregs) could make immunologic barriers against CD8 + T cell-mediated antitumor immune responses. Thus, CD8 + T cells are needed to be primed and activated toward effector CTLs in a process called tumor immunity cycle for making durable and efficient antitumor immune responses. The CD8 + T cell priming is directed essentially as a corroboration work between cells of innate immunity including dendritic cells (DCs) and natural killer (NK) cells with CD4 + T cells in adoptive immunity. Upon activation, effector CTLs infiltrate to the core or invading site of the tumor (so-called infiltrated-inflamed [I-I] TME) and take essential roles for killing cancer cells. Exogenous reactivation and/or priming of CD8 + T cells can be possible using rational immunotherapy strategies. The increase of the ratio for costimulatory to coinhibitory mediators using immune checkpoint blockade (ICB) approach. Programmed death-1 receptor (PD-1)-ligand (PD-L1) and CTL-associated antigen 4 (CTLA-4) are checkpoint receptors that can be targeted for relieving exhaustion of CD8 + T cells and renewing their priming, respectively, and thereby eliminating antigen-expressing cancer cells. Due to a diverse relation between CTLs with Tregs, the Treg activity could be dampened for increasing the number and rescuing the functional potential of CTLs to induce immunosensitivity of cancer cells.CD8+ cytotoxic T lymphocytes (CTLs) are preferred immune cells for targeting cancer. During cancer progression, CTLs encounter dysfunction and exhaustion due to immunerelated tolerance and immunosuppression within the tumor microenvironment (TME), with all favor adaptive immune-resistance. Cancer-associated fibroblasts (CAFs), macrophage type 2 (M2) cells, and regulatory T cells (Tregs) could make immunologic barriers against CD8 + T cell-mediated antitumor immune responses. Thus, CD8 + T cells are needed to be primed and activated toward effector CTLs in a process called tumor immunity cycle for making durable and efficient antitumor immune responses. The CD8 + T cell priming is directed essentially as a corroboration work between cells of innate immunity including dendritic cells (DCs) and natural killer (NK) cells with CD4 + T cells in adoptive immunity. Upon activation, effector CTLs infiltrate to the core or invading site of the tumor (so-called infiltrated-inflamed [I-I] TME) and take essential roles for killing cancer cells. Exogenous reactivation and/or priming of CD8 + T cells can be possible using rational immunotherapy strategies. The increase of the ratio for costimulatory to coinhibitory mediators using immune checkpoint blockade (ICB) approach. Programmed death-1 receptor (PD-1)-ligand (PD-L1) and CTL-associated antigen 4 (CTLA-4) are checkpoint receptors that can be targeted for relieving exhaustion of CD8 + T cells and renewing their priming, respectively, and thereby eliminating antigen-expressing cancer cells. Due to a diverse relation between CTLs with Tregs, the Treg activity could be dampened for increasing the number and rescuing the functional potential of CTLs to induce immunosensitivity of cancer cells. |
| Author | Najafi, Masoud Mortezaee, Keywan Farhood, Bagher |
| Author_xml | – sequence: 1 givenname: Bagher surname: Farhood fullname: Farhood, Bagher organization: Kashan University of Medical Sciences – sequence: 2 givenname: Masoud surname: Najafi fullname: Najafi, Masoud organization: School of Paramedical Sciences, Kermanshah University of Medical Sciences – sequence: 3 givenname: Keywan orcidid: 0000-0003-2004-3465 surname: Mortezaee fullname: Mortezaee, Keywan email: keywan987@yahoo.com, mortezaee.k@muk.ac.ir organization: School of Medicine, Kurdistan University of Medical Sciences |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/30520029$$D View this record in MEDLINE/PubMed |
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| Snippet | CD8+ cytotoxic T lymphocytes (CTLs) are preferred immune cells for targeting cancer. During cancer progression, CTLs encounter dysfunction and exhaustion due... CD8 + cytotoxic T lymphocytes (CTLs) are preferred immune cells for targeting cancer. During cancer progression, CTLs encounter dysfunction and exhaustion due... CD8 cytotoxic T lymphocytes (CTLs) are preferred immune cells for targeting cancer. During cancer progression, CTLs encounter dysfunction and exhaustion due to... |
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| SubjectTerms | Animals Antigens Antineoplastic Agents, Immunological - adverse effects Antineoplastic Agents, Immunological - therapeutic use Antitumor activity Apoptosis Cancer cancer cells Cancer immunotherapy CD4 antigen CD8 antigen CD8+ cytotoxic T lymphocytes (CTLs) Cell activation Cell Communication - drug effects CTL‐associated antigen 4 (CTLA‐4) Cytokines - metabolism Cytotoxicity Dendritic cells dendritic cells (DCs) Exhaustion Fibroblasts Humans Immune checkpoint Immune system Immunity Immunological tolerance Immunoregulation Immunosuppression Immunotherapy Immunotherapy - adverse effects Inflammation Innate immunity interferon‐γ (IFN‐γ) Lymphocyte Activation - drug effects Lymphocytes Lymphocytes T Lymphocytes, Tumor-Infiltrating - drug effects Lymphocytes, Tumor-Infiltrating - immunology Lymphocytes, Tumor-Infiltrating - metabolism Macrophages Natural killer cells Neoplasms - immunology Neoplasms - metabolism Neoplasms - pathology Neoplasms - therapy PD-1 protein PD-L1 protein Priming programmed death‐1 receptor (PD‐1)–ligand (PD‐L1) Receptors regulatory T cells (Tregs) Signal Transduction T-Lymphocytes, Cytotoxic - drug effects T-Lymphocytes, Cytotoxic - immunology T-Lymphocytes, Cytotoxic - metabolism Tumor Escape - drug effects Tumor Microenvironment tumor microenvironment (TME) Tumors |
| Title | CD8+ cytotoxic T lymphocytes in cancer immunotherapy: A review |
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